Phosphorylation within the cysteine-rich region of dystrophin enhances its association with β-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting.

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Published in Hum Mol Genet on July 31, 2014

Authors

Kristy Swiderski1, Scott A Shaffer2, Byron Gallis2, Guy L Odom3, Andrea L Arnett3, J Scott Edgar2, Dale M Baum4, Annabel Chee4, Timur Naim4, Paul Gregorevic5, Kate T Murphy4, James Moody6, David R Goodlett2, Gordon S Lynch4, Jeffrey S Chamberlain7

Author Affiliations

1: Basic and Clinical Myology Laboratory, Department of Physiology, University of Melbourne, VIC 3010, Australia Department of Neurology, University of Washington School of Medicine, Seattle, WA 98195-7720, USA.
2: Department of Medicinal Chemistry, University of Washington School of Medicine, Seattle, WA 98195-7610, USA.
3: Department of Neurology, University of Washington School of Medicine, Seattle, WA 98195-7720, USA.
4: Basic and Clinical Myology Laboratory, Department of Physiology, University of Melbourne, VIC 3010, Australia.
5: Muscle Biology and Therapeutics Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
6: Department of Biochemistry, University of Washington School of Medicine, Seattle, WA 98195-7350, USA and Program in Molecular and Cellular Biology, University of Washington School of Medicine, Seattle, WA 98195-7275, USA.
7: Department of Neurology, University of Washington School of Medicine, Seattle, WA 98195-7720, USA Department of Biochemistry, University of Washington School of Medicine, Seattle, WA 98195-7350, USA and Program in Molecular and Cellular Biology, University of Washington School of Medicine, Seattle, WA 98195-7275, USA jsc5@uw.edu.

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